3. INTRODUCTION
Salivary glands are important exocrine glands
Their prime function being secretion of saliva
Tumors of salivary glands represent 2 to 4 %
of head and neck neoplasms
They are broadly classified into benign and
malignant tumors
4. 70% of salivary gland tumors originate in
the parotid gland
8 % in the submandibular glands
22 % in the minor salivary glands and
sublingual
5. 75% of parotid tumors are benign
50% of tumors of submandibular and 60-80%
of minor salivary gland tumors are malignant
Pleomorphic adenomas are the most
common benign tumors comprising 85 % of
all salivary gland neoplasms
6. CLASSIFICATION
Salivary gland diseases vary in their incidence
and they are usually classified into
Neoplastic
Non-neoplastic
12. CLASSIFICATION OF SALIVARY
GLAND NEOPLASMS
They are remarkable for their histologic
diversity
They include :
Benign
Malignant
They may be of epithelial, mesenchymal and
lymphoid origin
18. Benign epithelial tumors
o Pleomorphic adenoma
o Myoepithelioma
o Basal cell adenoma
o Warthins tumor
o Oncocytoma
o Canalicular adenoma
o Sebaceous adenoma
o Lymphadenoma
o Ductal papillomas
o cystadenoma
20. ETIOLOGY
1. VIRUSES : EBV – lymphoepithelial
carcinoma
2. RADIATION : high frequency of
mucoepidermoid carcinoma and warthins
tumor
3. OCCUPATION :
{Rubber, arsenic, plumbing, automobile and
cosmetics}
21. 4 LIFESTYLE AND NUTRITION
Smoking –Warthin’s tumor
Tobacco use and alcohol – no association
5 HORMONES
22. HISTOGENESIS
Histogenic concepts that were evolved were
Unicellular theory
Bicellular theory
Reverse cell hypothesis
Multicellular histogenetic concept
23. UNICELLULAR THEORY
Proposed that the neoplasm arise from their
adult differentiated counterparts of salivary
gland units
Theory was later rejected
* induction of neoplasm requires
dedifferentiation of already specialized cells
24. BICELLULAR THEORY :
Eversole in 1971
Semipleuripotential theory
Based on the embryonic development of
palatal minor salivary glands
Eversole observed existence of reverse cell
during embryogenesis of palatal salivary
glands
25.
26. Palatal minor salivary glands develop as
downgrowth of bilayered ducts
Inner layer develop from outer basal layer
These basal layer was considered as reverse
cells
Stem cells
They are confined to basal region and
thought to cause tumors
Rejected – lack of specificity
27. REVERSE CELL HYPOTHESIS :
Regezi and Batsakis i 1977
Proposed that differentiated cell types in
mature salivary glands are incapable of
undergoing neoplastic alteration
Stem (reverse )cells are solely at risk for
neoplastic transformation
28. MULTICELLULAR HISTOGENETIC CONCEPT
Dardick in 1991
Proposed that any of the cells found in the
normal salivary system could probably serve as
the precursor for neoplasm
Both in vitro and in vivo studies have shown
that mitotic figures are frequently seen in inner
cell layer
29.
30.
31. TUMOR PROGRESSION IN SALIVARY
GLAND TUMORS
Multistep process
Involves sequential accumulation of genetic
changes
It may progress in many ways
32. They are :
Malignant transformation of benign salivary
gland tumors
Progression from low grade to high grade
carcinoma
Dedifferentiation of a carcinoma to high
grade carcinoma with loss of original line of
differentiation
Stromal invasion
33. DEDIFFERENTIATION OF SALIVARY GLAND
TUMORS
Transformation of salivary gland carcinoma
to a high grade carcinoma in which the
original line of differentiation is no longer
evident
Acinic cell carcinoma – first to be reported
34. Dedifferentiated component could be a form of
o High grade carcinoma
o Poorly differentiated carcinoma
o Undifferentiated carcinoma
Other tumors reported were –
• Mucoepidermoid carcinoma
• Adenoid cystic carcinoma
• Myoepithelial carcinoma
• Salivary duct carcinoma
• Hyalinizing clear cell carcinoma
35. GENETIC COMPONENTS
Genetic changes that could mediate
dedifferentiation are p53 mutation, increased
cyclin D1 expression , loss of expression of Rb
protein and gene amplification